EFFECT OF ACETAZOLAMIDE ON SLEEPING TIME INDUCED WITH BARBITURATES IN MICE : POSSIBLE RELATIONSHIP BETWEEN BARBITURATE SLEEP AND BRAIN CARBONIC ANHYDRASE ACTIVITY

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When the mice were treated with acetazolamide (AZA) 30 min before the administration of pentobarbital, the sleeping time was prolonged. At the moment of awakening from sleep, no change in the brain level of pentobarbital was observed by the AZA pretreatment, which suggests the constant brain sensitivity to the barbiturate. At that time, the plasma level was lowered by the AZA pretreatment. Pentobarbital had no effect on a carbonic anhydrase activity in brain inhibited by AZA. The results similar to those were obtained also in thiopental and norhexobarbital. Thus it was inferred that the prolongation of barbiturate sleep in mice pretreated with AZA is due to a decrease in the rate of removal of the barbiturate from the brain, through brain carbonic anhydrase inhibition followed by the lowering of cerebrospinal fluid flow. Hexobarbital sleeping time was shortened by the AZA pretreatment. At awakening, the brain hexobarbital level was somewhat, but not significantly, increased and the plasma level was significantly raised by the AZA pretreatment. Brain carbonic anhydrase inhibited by AZA was restored to control level with hexobarbital dosing. There seemed to be some particular interaction between AZA and hexobarbital in brain, which may be related to difference in barbiturate structures including N-methyl group.
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